Previous studies in our laboratory have shown a striking accumulation of i.v. pulsed radiolead by the choroid plexus and other barrier tissues. These results have suggested that selective barrier tissue dysfunction may occur in lead poisoning. We have now studied the effects of lead nitrate (10 to the minus 6th power M) on the in vitro accumulation of 3H-L-tyrosine by excised cat choroid plexus, hypothalamus, thalamus and caudate nucleus. The transport indices for 3H-L tyrosine in the brain regions were unaffected by lead whereas both the V max and Km values were significantly reduced for choroid (control vs. poisoned: Vmax equals .205 plus or minus .013 vs. .101 plus or minus .009 micron M/ml/min; P less than .01; Km equals .016 plus or minus .003 micron M vs. .005 plus or minus .001 micron M; P less than .01). These results demonstrate that lead can induce in vitro a selective dysfunction of the choroid plexus, a neural barrier tissue. Since tyrosine is a neuro-transmitter precursor, this effect may relate to the interactions of lead with central aminergic systems described by others, and thus may contribute to the pathogenesis of lead encephalopathy. We have also found that choroid plexus shows concentrative and temperature dependent accumulation of 45 Ca whereas the uptake of this solute by brain regions is not facilitated. We now plan a study of the effects of lead on choroid plexus 45 Ca accumulation, to see whether the metal also affects this choroidal function.